scholarly journals Role of prey subcellular distribution on the bioaccumulation of yttrium (Y) in the rainbow trout

2020 ◽  
Vol 258 ◽  
pp. 113804 ◽  
Author(s):  
Pierre-Yves Cardon ◽  
Olivier Roques ◽  
Antoine Caron ◽  
Maikel Rosabal ◽  
Claude Fortin ◽  
...  
2016 ◽  
Vol 53 ◽  
pp. 75
Author(s):  
Fumio Takizawa ◽  
Zhen Xu ◽  
David Parra ◽  
Daniela Gomez ◽  
Scott LaPatra ◽  
...  

2021 ◽  
Vol 38 (3) ◽  
pp. 269-273
Author(s):  
Mehmet Reşit Taysı ◽  
Muammer Kırıcı ◽  
Mahinur Kırıcı ◽  
Hasan Ulusal ◽  
Bünyamin Söğüt ◽  
...  

The aim of this study was to determine oxidative stress caused by mercury chloride (HgCl2) in rainbow trout (Oncorhynchus mykiss) liver tissue. For this purpose, the LD50 value of HgCl2 on rainbow trout was determined as 551 μg/L. In the study, 40 fish in four groups were exposed to 25% and 50% (138 and 276 µg/L) of the two subletal doses of HgCl2 for 2 and 7 days, with 10 fish (n=10) in each group. To determine oxidative stress; peroxynitrite (ONOO−), total oxidant level (TOS), total antioxidant level (TAS), oxidative stress index (OSI) and malondialdehyde (MDA) were analyzed. In the study, it was observed that the differences between the groups in terms of ONOO−, TOS, TAS and OSI levels in the liver tissues was significant (P<0.05), however, this difference was not significant (P>0.05) in terms of MDA values. As a result, it can be concluded that HgCl2 increases ONOO−, TOS, TAS, OSI and MDA levels in liver tissue and even small doses of mercury are toxic to fish.


1999 ◽  
Vol 18 (5) ◽  
pp. 938-945
Author(s):  
Henryka Dabrowska ◽  
Susan W. Fisher ◽  
Konrad Dabrowski ◽  
Alfred E. Staubus

1989 ◽  
Vol 147 (1) ◽  
pp. 471-491 ◽  
Author(s):  
D. G. MCDONALD ◽  
Y. TANG ◽  
R. G. BOUTILIER

Rainbow trout, fitted with arterial catheters, were exercised to exhaustion by manual chasing and then injected with either saline (controls), the β-agonist isoproterenol or the β-antagonist propranolol. Blood acid-base status, branchial unidirectional and net fluxes of Na+ and Cl−, and net fluxes of ammonia and acidic equivalents (JHnet) were monitored over the subsequent 4 h of recovery. These same parameters were also monitored in normoxic, resting fish following isoproterenol injection and in exercised fish following acute post-exercise elevation of external NaCl concentration. In addition to confirming an important role for β-adrenoreceptors in the regulation of branchial gas exchange and red cell oxygenation and acid-base status, we find a significant β-adrenergic involvement in the flux of lactic acid from muscle and in JHnet across the gills. Both isoproterenol infusion (into nonexercised fish) and exhaustive exercise were found to cause net acid excretion. The post-exercise JHnet was further augmented by elevating [NaCl] but was not affected, in this instance, either by β-stimulation or blockade, indicating that JHnet was not entirely regulated by a β-adrenergic mechanism. On the basis of a detailed analysis of unidirectional Na+ and Cl− fluxes, we conclude that the increase in JHnet following exercise arose mainly from increased Na+/H+(NH4+) exchange and that the upper limit on JHnet was set by the supply of external counterions and by the increase in branchial ionic permeability that invariably accompanies exhaustive exercise.


2000 ◽  
Vol 278 (4) ◽  
pp. R956-R963 ◽  
Author(s):  
Jean-Michel Weber ◽  
Deena S. Shanghavi

The rate of hepatic glucose production (Ra glucose) of rainbow trout ( Oncorhynchus mykiss) was measured in vivo by continuous infusion of [6-3H]glucose and in vitro on isolated hepatocytes to examine the role of epinephrine (Epi) in its regulation. By elevating Epi concentration and/or blocking β-adrenoreceptors with propranolol (Prop), our goals were to investigate the mechanism for Epi-induced hyperglycemia to determine the possible role played by basal Epi concentration in maintaining resting Ra glucose and to assess indirect effects of Epi in the intact animal. In vivo infusion of Epi caused hyperglycemia (3.75 ± 0.16 to 8.75 ± 0.54 mM) and a twofold increase in Ra glucose (6.57 ± 0.79 to 13.30 ± 1.78 μmol ⋅ kg− 1 ⋅ min− 1, n = 7), whereas Prop infusion decreased Ra from 7.65 ± 0.92 to 4.10 ± 0.56 μmol ⋅ kg− 1 ⋅ min− 1( n = 10). Isolated hepatocytes increased glucose production when treated with Epi, and this response was abolished in the presence of Prop. We conclude that Epi-induced trout hyperglycemia is entirely caused by an increase in Ra glucose, because the decrease in the rate of glucose disappearance normally seen in mammals does not occur in trout. Basal circulating levels of Epi are involved in maintaining resting Ra glucose. Epi stimulates in vitro glucose production in a dose-dependent manner, and its effects are mainly mediated by β-adrenoreceptors. Isolated trout hepatocytes produce glucose at one-half the basal rate measured in vivo, even when diet, temperature, and body size are standardized, and basal circulating Epi is responsible for part of this discrepancy. The relative increase in Ra glucose after Epi stimulation is similar in vivo and in vitro, suggesting that indirect in vivo effects of Epi, such as changes in hepatic blood flow or in other circulating hormones, do not play an important role in the regulation of glucose production in trout.


1999 ◽  
Vol 163 (1) ◽  
pp. 87-97 ◽  
Author(s):  
J Chyb ◽  
T Mikolajczyk ◽  
B Breton

In order to determine the factors of ovarian origin which can modulate the postovulatory secretion of the FSH-like gonadotropin (GtH I) and the LH-like gonadotropin (GtH II), freshly ovulated female rainbow trout were divided into two groups. In the first group the fish were stripped in order to eliminate the eggs and ovarian fluid from the body cavity, while in the second group the eggs were kept in the body cavity. Subsequently, fish from both groups were implanted with testosterone (10 mg/kg), 17beta-estradiol (10 mg/kg) or 17,20beta-ddihydroxy-4-regnen-3-one (17,20betaP) (1 mg/kg) or injected every 2 days with desteroidized ovarian fluid (1.5 ml/kg). The secretion of GtH I dramatically increased in stripped fish, reaching its maximum levels 2 weeks after ovulation. The preservation of eggs in the body cavity led to the suppression of this increase. The profiles of GtH II secretion were opposite to those encountered for GtH I because the increase of GtH II was observed only in unstripped fish. The administration of steroids showed that testosterone is able to inhibit GtH I release and stimulate that of GtH II in stripped fish, having no effect on the release of these gonadotropins in non-stripped animals. 17beta-Estradiol failed to modify GtH I secretion, however it decreased the release of GtH II in fish containing retained eggs in the body cavity. 17,20betaP had a delayed stimulating influence on GtH I release in unstripped fish. Finally, multiple injections of desteroidized ovarian fluid into stripped fish led to a significant decrease of GtH I release and to an increase of GtH II secretion. This study demonstrates that factors, which are present in ovarian fluid, modulate the post-ovulatory secretion of both gonadotropins--their net action is negative on GtH I and positive on GtH II. Among the steroids, testosterone is of major importance, being able to inhibit GtH I release and to stimulate that of GtH II. We also show that non-steroidal factors present in the ovarian fluid can influence the release of both gonadotropins, which indirectly supports the previous findings about the existence of inhibin/activin-like factors in fish.


2019 ◽  
Vol 27 (6) ◽  
pp. 1667-1671 ◽  
Author(s):  
Vasco Menconi ◽  
Paolo Pastorino ◽  
Giulia Cavazza ◽  
Morena Santi ◽  
Davide Mugetti ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document